GUT AND MUSCLE-TISSUE PO2 IN ENDOTOXEMIC DOGS DURING SHOCK AND RESUSCITATION

There is indirect evidence that tissue hypoxia occurs in human sepsis and surface measures of muscle tissue PO2 (Pti(O2)) in hypodynamic end otoxic animals are decreased. This study assessed systemic and regiona l tissue oxygenation in a more relevant model of hyperdynamic endotoxi cosis. We isolated venous outflow from the left hindlimb and a segment of ileum in six anesthetized dogs to measure muscle and gut O-2 deliv ery and uptake (VO2) and lactate flux, gut intramucosal pH (pH(i)) by tonometry, and Pti(O2) by multipoint surface electrodes placed on muco sal and serosal surfaces of gut and on muscle. We then infused Escheri chia coli lipopolysaccharide (LPS; 2 mg/kg) over 1 h followed by a 2-h infusion of dextran (0.5 mi kg(-1) min(-1)). LPS infusion significant ly decreased systemic and gut VO2, cardiac output (Q), and blood press ure and increased arterial lactate and gut lactate flux. Resuscitation increased and to above baseline and restored systemic VO2. In respons e to LPS and then resuscitation, muscle Pti(O2) distribution did not c hange, suggesting little microcirculatory disturbance, although mean P ti(O2) first decreased and then increased. In contrast, gut V-O2 and p H(i) remained low and lactate output remained high, despite restoratio n of gut blood flow. Gut VO2 lactate flux, pH(i), and Pti(O2) histogra ms were consistent with a marked redistribution of blood flow within t he gut wall, away from the mucosa and toward the muscularis. These dat a show that, in hyperdynamic acute endotoxemia, skeletal muscle Pti(O2 ) and VO2 are well maintained, but blood flow within the gut is signif icantly disturbed with mucosal hypoxia.